Levels (7.01 ?0.01 vs 6.93 ?0.04, P < 0.04 and 10.2 ?0.14 vs 7.3 ?0.14

Levels (7.01 ?0.01 vs 6.93 ?0.04, P < 0.04 and 10.2 ?0.14 vs 7.3 ?0.14 mmol/l, P < 0.03, respectively). Conclusions Antiplatelet drugs may have a beneficial effect in systemic inflammation and sepsis, and could be a novel therapy option, at least in patients of low bleeding risk. One mechanism of their effects could be a reduction in the microvascular thrombus formation.Oxygenation index.Figure 2 (abstract P28)Survival proportion. SCritical CareMarch 2007 Vol 11 Suppl27th International Symposium on Intensive Care and Emergency Medicinesimilar in all groups. While the oxygenation index (paO2/FiO2) decreased in all groups, group PH had the lowest values after 6 hours and throughout the rest of the experiments (P < 0.05) (Figure 1). Survival was lowest in group PH, followed by group P, while all animals in the control groups survived until 24 hours (Figure 2). Conclusion High-volume administration decreased oxygenation and survival in peritonitis but not in control animals. A high-volume approach may not be generally beneficial in abdominal sepsis. Reference 1. Rivers E, et al.: N Engl J Med 2001, 345:1368-1377.and high mortality. The impact of aggressive and prolonged volume administration on hepatosplanchnic oxygenation and mitochondrial function in human sepsis should be determined.P30 Effect of GDC-0834 (S-enantiomer) site C1-esterase inhibitor treatment on microcirculatory perfusion after superior mesenteric artery ischemiaM Lauterbach, G Horstick, N Plum, J Lotz, E Lauterbach, L Weilemann, O Kempski University Hospital Mainz, Germany Critical Care 2007, 11(Suppl 2):P30 (doi: 10.1186/cc5190) Multiple studies have stressed PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/20801496 the importance of the contribution of activated complement to the pathology of reperfusion injury just after tissue ischemia. Working with intravital microscopy, this study explores functional consequences of your inhibition in the classical pathway of complement activation with C1-esterase inhibitor (C1-INH) inside the context of superior mesenteric artery occlusion (SMAO)/ reperfusion. Thirty anesthetized, spontaneously breathing, male Sprague?Dawley rats underwent SMAO for 60 minutes followed by reperfusion (four hours). C1-esterase inhibitor (100 IU/kg, 200 IU/kg body weight) or saline (0.9 ) was given as a single bolus ahead of reperfusion. Sham-operated animals (n = 10) without SMAO served as controls. Systemic hemodynamics had been monitored continuously, arterial blood gases analyzed intermittently, and leukocyte/ endothelial interactions in the mesenteric microcirculation quantified at intervals using intravital microscopy. Ileal lipid-binding protein (I-LBP) levels had been measured from serum samples with an ELISA at the end from the experiments. C1-INH restored microcirculatory perfusion of postcapillary venules to baseline levels inside a dose-dependent manner and reduced leukocyte adhesion following SMAO/reperfusion to similar levels in each C1-INH-treated groups for the duration of reperfusion. Furthermore, C1INH therapy effectively prevented metabolic acidosis, and reduced the will need for intravenous fluids to support blood stress. Additionally, I-LBP levels decreased inside a dose-dependent manner, and were comparable with the levels of sham-operated animals at the end from the experiments. Survival prices were one hundred in controls and immediately after 200 IU/kg C1-INH, 90 immediately after one hundred IU/kg C1-INH, and 30 in saline-treated animals. Inside the setting of mesenteric ischemia, C1-INH given as a bolus infusion shortly just before reperfusion effectively restored microcirculatory perfusion within a dose-dependent m.